兔膝骨性关节炎软骨损伤及降钙素的保护作用

目的:探讨兔膝骨性关节炎(KOA)时的软骨损伤及降钙素(CT)的保护作用.方法:将36只健康大耳白兔随机分为空白对照组(A组)、模型组(B组)和CT治疗组(C组),B、C组采用改良Hulth法复制膝骨性关节炎模型,A组除切开皮肤和关节腔外,不做其他处理,从术后第6周开始C组每天皮下注射CT 5 U/kg,A、B组给与等量生理盐水皮下注射,连续注射20d后处死动物.观察关节软骨病理组织学和关节液肿瘤坏死因子(TNF)-α、一氧化氮(NO)及关节软骨Ⅱ型胶原及基质金属蛋白酶(MMP)-1的变化,以及降钙素对上述指标的影响.结果:与A组相比较,B组JP和Mankin’S评分升高,关节软骨损伤加重,关节液中TNF-α、NO水平升高(P＜0.05),关节软骨Ⅱ型胶原含量降低,MMP-1活性升高(P＜0.05)；与B组相比,C组关节液中TNF-α、NO水平降低(P＜0.05),关节软骨损伤减轻、Ⅱ型胶原含量升高,MMP-1活性降低(P＜0.05).结论:CT可能通过抑制TNF-α、NO的表达而对KOA软骨损伤起保护作用.

Effects of Calcitonin on Articular Cartilage Injury in Rabbits with Knee Osteoarthritis

Objective:To study effects of calcitonin (CT) on the articular cartilage injury in rabbits with knee osteoar thritis.Methods:Thirty-six rabbits were randomly divided into three groups,normal group (group A),model group (group B) and CT treatment group (group C).The modified Hulth ’ s method was used to establish the model of knee osteoarthritis in group B and group C.Except for incision of skin and articular cavity,there was no other treatment in group A.The rabbits in group C were treated by hypodermic injection CT (5 U/kg) everyday.The other rabbits were treated by the same dose of nor mal saline.Animals were sacrificed after 20 d injection.The pathomorphism and tumor necrosis factor (TNF)-α,nitric oxide (NO),collagen Ⅱ and MMP-1 were observed.The effect of calcitonin on the above indicator was also detected.Results:Compared with group A,scores of JP and Mankin were significantly higher,articular cartilage injury was more serious,con tents of TNF-α and NO in synovial fluid increased (P < 0.05) and the expression of MMP-1 increased,but the expression of collagen Ⅱ decreased (P < 0.05) in group B.Compared with group B,contents of TNF-α and NO in synovial fluid decreased significantly (P < 0.05),the articular cartilage injury relieved evidently,the expression of collagen Ⅱ increased significantly and the expression of MMP-1 decreased significantly in group C (P < 0.05).Conclusion:The protective effect of CT on artic ular cartilage injury was by inhibition of TNF-α and NO.